2-Deoxy-D-glucose (2-DG) Glycolysis inhibitor

Cat.No.S4701

An analog of glucose, 2-Deoxy-D-glucose (2-DG) is a glycolytic inhibitor with antiviral activity. It induces apoptosis and inhibits Herpes Simplex Virus type-1 (HSV-1) receptor expression.
2-Deoxy-D-glucose (2-DG) Carbohydrate Metabolism modulator Chemical Structure

Chemical Structure

Molecular Weight: 164.16

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 164.16 Formula

C6H12O5

Storage (From the date of receipt)
CAS No. 154-17-6 Download SDF Storage of Stock Solutions

Synonyms 2-deoxyglucose, NSC 15193, 2-Deoxy-D-arabino-hexose, D-Arabino-2-deoxyhexose Smiles C(C=O)C(C(C(CO)O)O)O

Solubility

In vitro
Batch:

DMSO : 500 mg/mL ( (3045.8 mM) Warmed with 50°C water bath; Ultrasonicated; Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Water : 83 mg/mL

Ethanol : 8 mg/mL

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Mass Concentration Volume Molecular Weight

In vivo
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Mechanism of Action

Targets/IC50/Ki
glycolysis [1]
In vitro
2-Deoxy-D-glucose (2-DG) activates AKT function through phosphatidylinositol 3-kinase (PI3K) and is independent of glycolysis or mTOR inhibition. Its treatments disrupt the binding between insulin-like growth factor 1 (IGF-1) and IGF-binding protein 3 (IGFBP3) so that the free form of IGF-1 could be released from the IGF-1·IGFBP3 complex to activate IGF-1 receptor (IGF1R) signaling. 2-DG-induced activation of many survival pathways can be jointly attenuated through IGF1R inhibition. This compound also induces time- and dose-dependent ERK phosphorylation[1]. It is readily transported into cells and is phosphorylated by hexokinase, but cannot be metabolized further and accumulates in the cell. This leads to ATP depletion and the induction of cell-death[2]. 2DG significantly suppresses proliferation, causes apoptosis and reduces migration of murine endothelial cells, inhibiting formation of lamellipodia and filopodia and causing disorganization of F-actin filaments in murine endothelial cell[5].
In vivo
Treatment of cancer patients with relatively high doses of 2-Deoxy-D-glucose (2-DG) (greater than 200 mg/kg) was largely ineffective in managing tumor growth. Side effects of this compound included elevated blood glucose levels, progressive weight loss with lethargy, and behavioral symptoms of hypoglycemia[2]. It enhances isoflurane-induced loss of righting reflex in mice. By reducing metabolism, 2-DG treatment can decrease body temperature in rodent, enhancing sensitivity to anesthetics[3]. A diet containing it significantly increased serum ketone body level and brain expression of enzymes required for ketone body metabolism. The 2-DG-induced maintenance of mitochondrial bioenergetics was paralleled by simultaneous reduction in oxidative stress. Further, treated mice exhibited a significant reduction of both amyloid precursor protein (APP) and amyloid beta (Aβ) oligomers, which was paralleled by significantly increased α-secretase and decreased γ-secretase expression, indicating that this compound induced a shift towards a non-amyloidogenic pathway. It increased expression of genes involved in Aβ clearance pathways, degradation, sequestering, and transport. Concomitant with increased bioenergetic capacity and reduced β-amyloid burden, 2-DG significantly increased expression of neurotrophic growth factors, BDNF and NGF, thus reduces pathology in female mouse model of Alzheimer's disease[4].
References
  • https://pubmed.ncbi.nlm.nih.gov/21747957/
  • https://pubmed.ncbi.nlm.nih.gov/26398947/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT02558140 Completed
Neoplasms
Hoffmann-La Roche
October 11 2015 Phase 1
NCT01998841 Completed
Alzheimer''s Disease
Genentech Inc.|Banner Alzheimer''s Institute|National Institute on Aging (NIA)
December 20 2013 Phase 2

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